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    Home > Food News > Food Articles > Anti-age mice: Hair loss, wrinkles may be saved

    Anti-age mice: Hair loss, wrinkles may be saved

    • Last Update: 2021-03-12
    • Source: Internet
    • Author: User
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    Journal:
    Bhupendra Singh et al
    Published: 2018/7/18
    Digital Identification Number: 10.1186/s41419-018-0765-9
    Original link:A recent study found that restoring mitochondrial DNA to normal levels can reverse signs of aging in mice, such as hair loss and wrinkles. This research may in turn lead to a number of related in-depth studies, which are exciting for human health.and hair loss are associated with significant changes in human aging. Keshav Singh's team published a study on
    in a recent issue of the Journal of Aging. They found that in mice, wrinkles and hair loss caused by missing mitochondrial DNA (mtDNA) could be achieved by inhibiting co-expression of the POLG1 mutation, which can lead to a reduction in mitochondrial DNA in tissues. Although the study is still in its early stages, its significance lies in establishing a link between mitochondrial DNA and signs of aging, which can be reversed by restoring mitochondrial DNA levels. This offers a wide range of possibilities for the treatment of aging-related conditions.
    mitochondrials are cells that produce energy in cells, also known as "cell power plants." Past studies have found that mitochondrial dysfunction can cause many diseases, most of which are associated with mitochondrial oxyphosphation (OXPHOS) dysfunction. Cells use enzymes to oxidize nutrients through the OXPHOS process in mitochondrials and produce large amounts of adenosine triphosphate (ATP) as the main source of energy. In the process of aging, the decline of the overall function of mitochondrials is widely reported. In addition, mitochondrial dysfunction, which usually causes a decrease in mitochondrial DNA, can lead to other potential aging-related conditions, such as cancer, Parkinson's disease, and Alzheimer's disease.
    To study the role of mitochondrial DNA in aging and various conditions, Keshav Sing's team created a mouse model that could produce mice with mitochondrial DNA loss by controlling the expression of gamma polymerases needed for mitochondrial function. Interestingly, wrinkles and hair loss, important early traits associated with aging, also occur in mice with mitochondrial dysfunction. Most thought-provokingly, the researchers found that mitochondrial dysfunction could be reversed if gamma polymerase function was restored.mouse model of mitochondrial DNA loss used in this study could also be used to quickly identify disease genes and path pathlines associated with mitochondrial DNA. In addition, this animal model is expected to alter mitochondrial DNA levels in specific tissues of different organs, and may therefore be used to study the role of mitochondrials in the aging process or other mitochondrial-related diseases in the body. The mouse model provides an unprecedented opportunity to develop drugs to combat aging-related skin and hair problems (e.g. wrinkles, hair loss, inflammation, etc.) and other mitochondrial dysfunction-related diseases by enhancing mitochondrial function.
    summary:
    Mitochondrial DNA (mtDNA) depletion is involved in mtDNA depletion syndromes, mitochondrial diseases, aging and aging-associated chronic diseases, and other human pathologies. To evaluate the consequences of depletion of mtDNA in the whole animal, we created an inducible mtDNA-depleter mouse expressing, in the polymerase domain of POLG1, a dominant-negative mutation to induce depletion of mtDNA in various tissues. These mice showed reduced mtDNA content, reduced mitochondrial gene expression, and instability of supercomplexes involved in oxidative phosphorylation (OXPHOS) resulting in reduced OXPHOS enzymatic activities. We demonstrate that ubiquitous depletion of mtDNA in mice leads to predominant and profound effects on the skin resulting in wrinkles and visual hair loss with an increased number of dysfunctional hair follicles and inflammatory responses. Development of skin wrinkle was associated with the significant epidermal hyperplasia, hyperkeratosis, increased expression of matrix metalloproteinases, and decreased expression of matrix metalloproteinase inhibitor TIMP1. We also discovered markedly increased skin inflammation that appears to be a contributing factor in skin pathology. Histopathologic analyses revealed dysfunctional hair follicles. mtDNA-depleter mice also show changes in expression of aging-associated markers including IGF1R, KLOTHO, VEGF, and MRPS5. mtDNA-repleter mice showed that, by turning off the mutant POLG1 transgene expression, mitochondrial function, as well as the skin and hair pathology, is reversed to wild-type level. To our knowledge that restoration of mitochondrial functions can reverse the skin and hair pathology is unprecedented.
    (Source: Science.com)
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